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EIF2AK2 activates autophagy via JAK2/STAT3 pathway to promote oral squamous cell carcinoma malignancy

Xiaonan Zhang1, Xiangling Liao2, Zhen Du1

  • 1Department of Stomatology, Beijing Luhe Hospital, Capital Medical University, No. 82 Xinhua South Road, Tongzhou District, Beijing, 101100, China.

Odontology
|January 7, 2026
PubMed

Insights

EIF2AK2 is overexpressed in oral squamous cell carcinoma (OSCC), promoting cancer growth and spread. Inhibiting EIF2AK2 reduces OSCC malignancy and autophagy by affecting the JAK2/STAT3 pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Oral squamous cell carcinoma (OSCC) is a prevalent malignancy.
  • EIF2AK2 dysregulation is linked to OSCC progression, but mechanisms remain unclear.

Purpose of the Study:

  • To investigate the role and mechanisms of EIF2AK2 in OSCC progression.
  • To determine EIF2AK2's impact on OSCC malignant characteristics, autophagy, and molecular pathways.

Main Methods:

  • Analysis of EIF2AK2 expression in OSCC tissues and cell lines.
  • EIF2AK2 knockdown using siRNA and in vitro functional assays.
  • Assessment of autophagy markers and the JAK2/STAT3 signaling pathway.

Main Results:

  • EIF2AK2 is significantly overexpressed in OSCC.
  • EIF2AK2 knockdown suppressed OSCC proliferation, migration, and invasion, and inhibited EMT.
  • EIF2AK2 inhibition reduced autophagy and downregulated the JAK2/STAT3 axis.

Conclusions:

  • EIF2AK2 acts as an oncogene in OSCC progression.
  • EIF2AK2 promotes OSCC malignancy by activating autophagy via the JAK2/STAT3 pathway.
Keywords:
EIF2AK2EMTJAK2/STAT3Migration and invasionOral squamous cell carcinoma

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